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Eight groups of 1-day-old or 8-week-old chickens were exposed by contact to lymphoid leukosis virus (LLV) infection. Five groups of about 60 spf chickens were used. Three groups of the same size were progeny from LLV vaccinated hens. Five groups were housed in one chicken house in close contact with a large number of immunologically tolerant chickens (virus "spreaders"). On two occasions infectious LLV was recovered from air/dust samples collected in this house. In the second house a small number of congenitally infected birds generated a mild degree of LLV exposure. It was demonstrated that infection by contact may lead to lymphoma formation and congenital virus transmission. The incidence of virus infection and LL mortality in the groups of birds exposed at 8 weeks of age were significantly lower than in chickens exposed at 1 day of age. In addition, about 100-fold differences in numbers of LLV-associated white blood cells were observed between both age groups. These results indicate that in addition to resistance to tumour formation, resistance to LLV infection develops in the chicken with increasing age. Maternal antibodies, present in three groups exposed at 1 day of age, reduced the rate of infection and the incidence of LL.

SUMMARYViraemia and neutralising antibodies were determined in chickens of six age-groups following inoculation with leukosis virus of subgroups A and B at the age of 1 day, and 2, 4, 6, 8 and 10 weeks respectively. The birds were kept in a filtered air positive pressure (FAPP) house. A seventh agegroup, accommodated in a separate FAPP-house, was used as an untreated control.

SUMMARYA programme to develop resistance to Marek's disease (MD) in chickens in two non-inbred White Plymouth Rock (WPR) lines by breeding from survivors was initiated in 1968 and since then nine generations have been produced. In each generation only sires and dams which survived heavy exposure to virulent MD virus (MDV), Dutch strain K, either by inoculation (for the first two generations) or by contact-exposure (for the following seven generations) were used.In this long term trial a high level of resistance to MD was reached within five generations; thereafter no marked further increase in resistance could be obtained. Susceptibility to MD, reflected by MD mortality in each generation, was expressed as % incidence of MD.Statistical evaluation of MD susceptibility in the nine generations of the two lines revealed a significant interaction between MD mortality and two sources of variation, sex and generation. No overall line effect was found, but there was a significant line x generation interaction. The remaining interactions were not significant. Results indicate that breeding from survivors for development of resistance to MD is feasible. Exposure of birds to either artificial (by injection) or